Role of inflammation and inflammasome activation in human bile cast nephropathy

• DOI: 10.1111/nep.13696
• Publication Date: 2020-01-30T11:55:02Z
• Authors: Kurt T. K. Giuliani; Andrew J. Kassianos; Katrina Kildey; Anca Grivei; Xiangju Wang; Jacobus Ungerer; Leo Francis; Helen Healy; Pedro F. H. Gois
• Keywords: CD68; Pyroptosis

Bile cast nephropathy (BCN) is an underdiagnosed cause of acute kidney injury (AKI). The precise pathogenesis bilirubin tubular toxicity remains unknown. aim this study to explore the cellular and molecular pathophysiology human BCN. Paraffin-embedded sections renal biopsy tissue from a BCN patient were stained by immunohistochemistry (IHC) for oxidative stress (4-hydroxynonenal), immune cell subpopulations, including dendritic cells (CD1c), macrophages (CD68) T (CD3), inflammasome activation staining active-caspase-1 adaptor protein, ASC (apoptosis-associated speck-like protein containing caspase recruitment domain). Quantitative analyses IHC compared healthy cortical tissue. We identified yellow brown granular casts within case, consistent with presence bile pigment. pigment was associated strong 4-hydroxynonenal intensity, marker stress. Diffuse tubulointerstitial inflammatory infiltrate detected, elevated CD1c, CD68 CD3 staining. Foci activity co-localized intense infiltration, increased Our findings are first suggest that may lead trigger signalling cascade, leading interstitial inflammation driving AKI pathobiology. SUMMARY AT A GLANCE report suggests